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Neurotoxicity following intracerebral injection of mercury compounds

Neurotoxicity following intracerebral injection of mercury compounds
Neurotoxicity following intracerebral injection of mercury compounds

Mercury is a potent neurotoxin, but the clinical patterns of organic and inorganic mercury poisoning are very different. Methyl mercury produces a neurological disease; consistent signs include ataxia, dysarthria and constriction of visual fields. Inorganic mercury affects the gastro-intestinal, renal and nervous systems; gingivitis, stomatatis, tremors and psychiatric changes are common. Despite these apparent differences, recent systemic toxicity experiments suggest that the changes in dorsal root ganglia neurones are identical with the two compounds. To test this hypothesis, between 10-` and 10-~ mol of mercuric chloride and methyl mercuric acetate were injected directly into the cerebrum of rats. The histological changes were similar with the two compounds. Neuronal necrosis and cerebral oedema were the most prominent features. Control injections of sodium chloride, distilled water and buffers produced no significant changes. Ultrastructurally, neurones showed pronounced cytoplasmic swelling, suggesting a defect at the cell membrane level. Similar changes were seen with injections of ouabain, glutaraldehyde, mercury mixed with cysteine and blood from animals poisoned systemically with methyl mercury. This form of neuronal necrosis differs from that of systemic methyl mercury toxicity where the earliest changes are in the endoplasmic reticulum. This difference may be related to the higher local concentration and rate of accumulation of mercury after intracerebral injection. The comparative size of lesions was estimated anatomically, and by reference to blood brain barrier dysfunction. Inorganic lesions were only slightly larger than those produced by equimolar amounts of organic mercury. It has been suggested that the toxicity of organic mercurials is the result of biotransformation to inorganic mercury. If this is so, it is surprising that inorganic mercury lesions were not far larger.

University of Southampton
Gallagher, Patrick J
14c495ef-03bd-499e-8feb-b4d8fa4508cf
Gallagher, Patrick J
14c495ef-03bd-499e-8feb-b4d8fa4508cf

Gallagher, Patrick J (1978) Neurotoxicity following intracerebral injection of mercury compounds. University of Southampton, Doctoral Thesis.

Record type: Thesis (Doctoral)

Abstract

Mercury is a potent neurotoxin, but the clinical patterns of organic and inorganic mercury poisoning are very different. Methyl mercury produces a neurological disease; consistent signs include ataxia, dysarthria and constriction of visual fields. Inorganic mercury affects the gastro-intestinal, renal and nervous systems; gingivitis, stomatatis, tremors and psychiatric changes are common. Despite these apparent differences, recent systemic toxicity experiments suggest that the changes in dorsal root ganglia neurones are identical with the two compounds. To test this hypothesis, between 10-` and 10-~ mol of mercuric chloride and methyl mercuric acetate were injected directly into the cerebrum of rats. The histological changes were similar with the two compounds. Neuronal necrosis and cerebral oedema were the most prominent features. Control injections of sodium chloride, distilled water and buffers produced no significant changes. Ultrastructurally, neurones showed pronounced cytoplasmic swelling, suggesting a defect at the cell membrane level. Similar changes were seen with injections of ouabain, glutaraldehyde, mercury mixed with cysteine and blood from animals poisoned systemically with methyl mercury. This form of neuronal necrosis differs from that of systemic methyl mercury toxicity where the earliest changes are in the endoplasmic reticulum. This difference may be related to the higher local concentration and rate of accumulation of mercury after intracerebral injection. The comparative size of lesions was estimated anatomically, and by reference to blood brain barrier dysfunction. Inorganic lesions were only slightly larger than those produced by equimolar amounts of organic mercury. It has been suggested that the toxicity of organic mercurials is the result of biotransformation to inorganic mercury. If this is so, it is surprising that inorganic mercury lesions were not far larger.

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Published date: 1978

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Local EPrints ID: 463800
URI: http://eprints.soton.ac.uk/id/eprint/463800
PURE UUID: 1378f9fe-2072-4ffe-a68d-9ee40451d789

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Date deposited: 04 Jul 2022 20:57
Last modified: 04 Jul 2022 20:57

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Author: Patrick J Gallagher

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